IgE bound to the surface of mast cells and/or basophils is responsible for the immediate hypersensitivity reaction. This response once established, persists for prolonged periods of time. We have recently shown that the mechanism is not due to internalization (J. Immunol., in press). Cross linking of the IgE by allergen (or other means) is normally necessary to elicit cell degranulation, which results in histamine release. We wish to determine if analogous, chemically induced cross linking affects the fate of IgE compared to monomeric IgE.